In hematological malignancies, such as B cell malignancies, the role of HLA-G seems more complex and may depend on a balance between the HLA-G-driven inhibitory mechanism of antitumor responses and the antiproliferative effects on malignant B cells which will be under the control of ILT2 expression or of another as yet unknown receptor (Figure 2). This evidence concerns the gene HLA-G and hematologic disorder.